| Project/Area Number |
23790987
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Neurology
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| Research Institution | Nagoya University |
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Principal Investigator |
IIJIMA Masahiro 名古屋大学, 大学院・医学系研究科, COE 特任助教 (40437041)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 難治性ニューロパチー / 軸索-髄鞘間相互作用 / transient axoglial glycoprotein-1 (TAG-1) / 脱髄 / 軸索障害 / 脱髄（demyelination） / 軸索障害（axonal damage） / 軸索脆弱性 / 軸索－髄鞘相互作用 / TAG-1 / 実験的自己免疫性神経炎 / axon-glial interaction / ノックアウトマウス |
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| Research Abstract |
Axonal damage concomitant of inflammatory demyelination is one of the major factors for refractory or therapy-resistant peripheral neuropathies. In this study, we focused into transient axoglial glycoprotein-1 (TAG-1) which is related to axon-myelin interaction. We induced experimental autoimmune neuritis (EAN) on TAG-1 knockout (KO) mice and investigated phenotypes by clinicoelectrophysiological, and pathological analysis. As a result, the breakdown of the axon-myelin interaction could be associated to vulnerability of axonal function as well as refractory characteristics in inflammatory demyelinating neuropathies.
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